中华临床医师杂志(电子版)
中華臨床醫師雜誌(電子版)
중화림상의사잡지(전자판)
CHINESE JOURNAL OF CLINICIANS(ELECTRONIC VERSION)
2013年
22期
9931-9936
,共6页
邓超%李英%苏醒%曹玉芳%陈栩栩
鄧超%李英%囌醒%曹玉芳%陳栩栩
산초%리영%소성%조옥방%진허허
危重病%超声检查,多普勒%急性肾损伤%液体冲击%肾脏抵抗指数
危重病%超聲檢查,多普勒%急性腎損傷%液體遲擊%腎髒牴抗指數
위중병%초성검사,다보륵%급성신손상%액체충격%신장저항지수
Critical illness%Ultrasonography,Doppler%Acute kidney injury%Fluid responsiveness%Renal resistive index
目的:初步探讨溶液冲击治疗后肾脏抵抗指数的变化。方法前瞻性队列研究,纳入35例需要连续机械通气和大量输液治疗的ICU患者,大量输液治疗前后给予肾脏抵抗指数检测。肾脏多普勒检测肾脏抵抗指数,食管多普勒监测主动脉血流。结果35例ICU患者中,17例(49%)患者符合溶液冲击反应的条件,主动脉血流量至少增加10%。液体冲击后,平均动脉压力从73 mm Hg(四分位距68~79 mm Hg)上升到80 mm Hg(四分位距75~86 mm Hg)具有统计学差异(P<0.0001),心脏每搏量从50 ml(四分位距30~77 ml)增加到55 ml(39~84 ml),具有统计学差异(P<0.0001)。液体冲击后溶液冲击应答组中心脏每搏量改变了+28.6%(+18.8%~+38.8%),液体冲击非应答组的每搏量是+3.1%(-1.6%~+7.4%)。肾脏抵抗指数在溶液冲击治疗无应答前为0.72(0.67~0.75)和后0.71为0.67~0.75),未发生改变(P=0.62)。肾脏抵抗指数在溶液冲击应答前0.70为(0.65~0.75)和后为0.72(0.68~0.74),也未改变(P=0.11)。心脏每搏量与溶液冲击后抵抗指数之间无明显相关性(r2=0.04,P=0.25),包括溶液冲击应答者(r2=-0.02,P=0.61)和溶液冲击无应答者(r2=0.08,P=0.27)。心脏每搏量与亚组溶液冲击后抵抗指数改变是否伴有急性肾损伤无相关性。结论溶液冲击后全身血流动力学改变没有引起肾脏抵抗指数变化,与是否伴随急性肾损伤无相关性。
目的:初步探討溶液遲擊治療後腎髒牴抗指數的變化。方法前瞻性隊列研究,納入35例需要連續機械通氣和大量輸液治療的ICU患者,大量輸液治療前後給予腎髒牴抗指數檢測。腎髒多普勒檢測腎髒牴抗指數,食管多普勒鑑測主動脈血流。結果35例ICU患者中,17例(49%)患者符閤溶液遲擊反應的條件,主動脈血流量至少增加10%。液體遲擊後,平均動脈壓力從73 mm Hg(四分位距68~79 mm Hg)上升到80 mm Hg(四分位距75~86 mm Hg)具有統計學差異(P<0.0001),心髒每搏量從50 ml(四分位距30~77 ml)增加到55 ml(39~84 ml),具有統計學差異(P<0.0001)。液體遲擊後溶液遲擊應答組中心髒每搏量改變瞭+28.6%(+18.8%~+38.8%),液體遲擊非應答組的每搏量是+3.1%(-1.6%~+7.4%)。腎髒牴抗指數在溶液遲擊治療無應答前為0.72(0.67~0.75)和後0.71為0.67~0.75),未髮生改變(P=0.62)。腎髒牴抗指數在溶液遲擊應答前0.70為(0.65~0.75)和後為0.72(0.68~0.74),也未改變(P=0.11)。心髒每搏量與溶液遲擊後牴抗指數之間無明顯相關性(r2=0.04,P=0.25),包括溶液遲擊應答者(r2=-0.02,P=0.61)和溶液遲擊無應答者(r2=0.08,P=0.27)。心髒每搏量與亞組溶液遲擊後牴抗指數改變是否伴有急性腎損傷無相關性。結論溶液遲擊後全身血流動力學改變沒有引起腎髒牴抗指數變化,與是否伴隨急性腎損傷無相關性。
목적:초보탐토용액충격치료후신장저항지수적변화。방법전첨성대렬연구,납입35례수요련속궤계통기화대량수액치료적ICU환자,대량수액치료전후급여신장저항지수검측。신장다보륵검측신장저항지수,식관다보륵감측주동맥혈류。결과35례ICU환자중,17례(49%)환자부합용액충격반응적조건,주동맥혈류량지소증가10%。액체충격후,평균동맥압력종73 mm Hg(사분위거68~79 mm Hg)상승도80 mm Hg(사분위거75~86 mm Hg)구유통계학차이(P<0.0001),심장매박량종50 ml(사분위거30~77 ml)증가도55 ml(39~84 ml),구유통계학차이(P<0.0001)。액체충격후용액충격응답조중심장매박량개변료+28.6%(+18.8%~+38.8%),액체충격비응답조적매박량시+3.1%(-1.6%~+7.4%)。신장저항지수재용액충격치료무응답전위0.72(0.67~0.75)화후0.71위0.67~0.75),미발생개변(P=0.62)。신장저항지수재용액충격응답전0.70위(0.65~0.75)화후위0.72(0.68~0.74),야미개변(P=0.11)。심장매박량여용액충격후저항지수지간무명현상관성(r2=0.04,P=0.25),포괄용액충격응답자(r2=-0.02,P=0.61)화용액충격무응답자(r2=0.08,P=0.27)。심장매박량여아조용액충격후저항지수개변시부반유급성신손상무상관성。결론용액충격후전신혈류동역학개변몰유인기신장저항지수변화,여시부반수급성신손상무상관성。
Objective To assess renal resistive index variations in response to fluid challenge. Methods This is prospective cohort study, 30 patients with consecutive patients receiving mechanical ventilation and requiring a fluid challenge, which was measured resistive index before and after fluid challenge. Renal Doppler was used to measure resistive index and esophageal Doppler to monitor aortic blood flow. Results Of the 35 included patients, 17 (49%) met our definition for fluid challenge responsiveness, that is, had at least a 10% increase in aortic blood flow. After fluid challenge, mean arterial pressure increased from 73 mm Hg (interquartile range 68-79) to 80 mm Hg (75-86; P<0.0001) and stroke volume from 50 ml (30-77) to 55 ml (39-84; P<0.0001). Stroke volume changes after fluid challenge were +28.6% (+18.8% to+38.8%) in fluid challenge responders and +3.1%(-1.6%to 7.4%) in fluid challenge nonresponders. Renal resistive index was unchanged after fluid challenge in both nonresponders (0.72 [0.67-0.75] before and 0.71 [0.67-0.75] after fluid challenge;P=0.62) and responders (0.70 [0.65-0.75] before and 0.72 [0.68-0.74] after fluid challenge;P=0.11). Stroke volume showed no correlations with resistive index changes after fluid challenge in the overall population (r2=0.04, P=0.25), in fluid challenge responders (r2=-0.02, P=0.61), or in fluid challenge nonresponders (r2=0.08, P=0.27). Stroke volume did not correlate with resistive index changes after fluid challenge in the subgroups without acute kidney injury (AKIN definition), with transient acute kidney injury, or with persistent acute kidney injury. Conclusion Systemic hemodynamic changes induced by fluid challenge do not translate into resistive index variations in patients without acute kidney injury, with transient acute kidney injury, or with persistent acute kidney injury.